Fig. 7: Investigation of the CD1a dependency of the systemic effects of imiquimod application.
From: CD1a promotes systemic manifestations of skin inflammation
A Spleen weight (mg) measurements on day 8 by imiquimod treatment of wild-type (WT) and CD1a transgenic mice (CD1a) followed by treatment i.p. with mouse IgG1 isotype control or CD1a transgenic injected with the refined panel of anti-CD1a antibodies as in the schematic (Fig. 6A). B–E Flow cytometric analysis of spleen of mouse IgG1 isotype treated wild-type (WT) and CD1a transgenic (CD1a); and CD1a transgenic injected with the refined panel of anti-CD1a antibodies following the treatment model of administration. Splenic CD4 (B) and CD8 (C) T-cell CD69 expression was assessed and neutrophils (D) and eosinophils (E) were enumerated. F–H Blood cellular analysis of the blood of mouse IgG1 isotype treated wild-type (WT) and CD1a transgenic (CD1a); and CD1a transgenic injected with the refined panel of anti-CD1a antibodies following the treatment model of administration. Circulating T cells (F), neutrophils (G) and eosinophils (H) were enumerated. I Plasma cytokine levels of the blood of mouse IgG1 isotype treated wild-type (WT) and CD1a transgenic (CD1a); and CD1a transgenic injected with anti-CD1a antibodies following the treatment model of administration as measured by cytometric bead array. Mean ± SD is shown. n represents biologically independent animals in each group. One-way-ANOVA with Dunnett’s test, *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001, examined over 3 (A–H I. IL-9, IL-5, IL-22) or 4 (I IFNγ, IL-1β, MCP-1, IL-17a, IL-23) independent experiments. Exact p-values and group sizes are recorded in Supplementary Table 6. Source Data are provided as a Source Data file.
